Prolonged smoldering Douglas fir smoke inhalation augments respiratory resistances, stiffens the aorta, and curbs ejection fraction in hypercholesterolemic mice

Eden, Matthew; Matz, Jacob; Garg, Priya; Gonzalez, Mireia Perera; McElderry, Katherine; Wang, Siyan; Gollner, Michael J.; Oakes, Jessica M.; Bellini, Chiara

doi:10.1016/j.scitotenv.2022.160609

Cited by 6 publications

(13 citation statements)

References 107 publications

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“…120 Collectively, this evidence suggests that autonomic dysregulation following WFS exposure may heighten the sensitivity or exaggerate cardiovascular responses to proinflammatory triggers such as metabolic stress and sleep disturbance, thereby increasing both immediate and long-term vulnerability to CVD (Figure 1). 121 Inhaled Versus Deposited PM Dose Notwithstanding the convenience of PM concentration as a dose metric, respiratory rate depression due to expiratory braking and extended inhalation or exhalation times in mice exposed to laboratory-scale WFS smoke 122 advocate for considering the product of PM concentration and minute volume as a measure of inhaled dose when attempting to align findings from in vivo studies in animal models with epidemiological and clinical evidence. Ventilation requirements inferred from HR 123 likewise differ depending on the physical activity level in first responders and other individuals exposed to environmental WFS.…”

Section: Compendium On Environmental Impacts On Cardiovascular Health...mentioning

confidence: 99%

“…14 Although direct measurement of particle deposition and clearance remain challenging to date, dosimetry models that couple airflow simulations with particle transport facilitate prediction of regional deposition fractions. 122,[124][125][126] As an additional benefit, these computational tools enable incorporation of processes for particle transport, deposition, and clearance that are tailored to each species and, therefore, remain instrumental in establishing equivalent exposure conditions between animals and humans.…”

Section: Compendium On Environmental Impacts On Cardiovascular Health...mentioning

confidence: 99%

“…122 Based on this computer-aided experimental design, mice inhaled laboratory-scale WFS at a 22 mg/m 3 PM concentration for 2 h/d, 5 d/wk, and for 8 weeks. 122 Exposed mice experienced a linear increase in BP throughout the study and exhibited reduced LV ejection fraction at end point, associated with a significant increase of LV end systolic volume. 122 Collagen-driven thickening of the aortic wall reduced cyclic distensibility and limited the tissue capacity for energy storage, preventing the aorta from acting as a pressure reservoir during the cardiac cycle (Windkessel function).…”

Section: Chronic Exposurementioning

confidence: 99%

“…122 Collagen-driven thickening of the aortic wall reduced cyclic distensibility and limited the tissue capacity for energy storage, preventing the aorta from acting as a pressure reservoir during the cardiac cycle (Windkessel function). 122…”

Section: Chronic Exposurementioning

confidence: 99%

“…Notwithstanding the convenience of PM concentration as a dose metric, respiratory rate depression due to expiratory braking and extended inhalation or exhalation times in mice exposed to laboratory-scale WFS smoke 122 advocate for considering the product of PM concentration and minute volume as a measure of inhaled dose when attempting to align findings from in vivo studies in animal models with epidemiological and clinical evidence. Ventilation requirements inferred from HR 123 likewise differ depending on the physical activity level in first responders and other individuals exposed to environmental WFS.…”

Section: In Vivo Evidence From Animal Studiesmentioning

confidence: 99%

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Impact of Wildfires on Cardiovascular Health

Williams,

Perreault,

Yazbeck

et al. 2024

Circulation Research

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Wildfire smoke (WFS) is a mixture of respirable particulate matter, environmental gases, and other hazardous pollutants that originate from the unplanned burning of arid vegetation during wildfires. The increasing size and frequency of recent wildfires has escalated public and occupational health concerns regarding WFS inhalation, by either individuals living nearby and downstream an active fire or wildland firefighters and other workers that face unavoidable exposure because of their profession. In this review, we first synthesize current evidence from environmental, controlled, and interventional human exposure studies, to highlight positive associations between WFS inhalation and cardiovascular morbidity and mortality. Motivated by these findings, we discuss preventative measures and suggest interventions to mitigate the cardiovascular impact of wildfires. We then review animal and cell exposure studies to call attention on the pathophysiological processes that support the deterioration of cardiovascular tissues and organs in response to WFS inhalation. Acknowledging the challenges of integrating evidence across independent sources, we contextualize laboratory-scale exposure approaches according to the biological processes that they model and offer suggestions for ensuring relevance to the human condition. Noting that wildfires are significant contributors to ambient air pollution, we compare the biological responses triggered by WFS to those of other harmful pollutants. We also review evidence for how WFS inhalation may trigger mechanisms that have been proposed as mediators of adverse cardiovascular effects upon exposure to air pollution. We finally conclude by highlighting research areas that demand further consideration. Overall, we aspire for this work to serve as a catalyst for regulatory initiatives to mitigate the adverse cardiovascular effects of WFS inhalation in the community and alleviate the occupational risk in wildland firefighters.

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